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Background and study aims The majority of patients with symptomatic sterile walled-off necrosis can be treated conservatively. Although endoscopic transluminal drainage is often performed in case of persistent symptoms, post-procedural iatrogenic infection may occur. The aim of this study was to evaluate the clinical outcome after endoscopic transluminal drainage of symptomatic sterile walled-off necrosis. Patients and methods Retrospective, multicenter, open-label case series of 56 patients with necrotizing pancreatitis who were drained endoscopically for symptomatic sterile walled-off necrosis between July 2001 and August 2018 at two tertiary referral hospitals. Primary endpoint was development of clinically relevant post-procedural iatrogenic infection, defined as need for endoscopic transluminal necrosectomy. Secondary endpoints included mortality, total number of interventions, hospital stay and resolution of symptoms at one-year follow-up. Results Endoscopic transluminal drainage of sterile walled-off necrosis was performed in 56 patients (57% male, median age 55 years), who presented with symptoms of abdominal pain (71%), gastric outlet obstruction (45%), jaundice (20%) and failure to thrive (27%). Forty-one patients (73%) developed clinically relevant post-procedural iatrogenic infection, resulting in a medium number of 3 endoscopic, radiological and/or surgical interventions (IQR 2 - 4). Mortality rate was 2%. Median total hospital stay was 12 days (IQR 6 - 17). Resolution of symptoms was reported in 40 of 46 patients (87%) for whom long-term follow-up was available (median follow-up of 13 months, IQR 6 - 29). Conclusions Endoscopic transluminal drainage of symptomatic sterile walled-off necrosis resulted in high clinical success. Nonetheless, in the majority of patients, additional reinterventions were needed due to clinically relevant post-procedural iatrogenic infection.Functional and anatomical connection between the liver and the spleen is most clearly manifested in various pathological conditions of the liver (cirrhosis, hepatitis). The mechanisms of the interaction between the two organs are still poorly understood, as there have been practically no studies on the influence exerted by the spleen on the normal liver. Mature male Sprague-Dawley rats of 250-260 g body weight, 3 months old, were splenectomized. The highest numbers of Ki67+ hepatocytes in the liver of splenectomized rats were observed at 24 h after the surgery, simultaneously with the highest index of Ki67-positive hepatocytes. After surgical removal of the spleen, expression of certain genes in the liver tissues increased. A number of genes were upregulated in the liver at a single time point of 24 h, including Ccne1, Egf, Tnfa, Il6, Hgf, Met, Tgfb1r2 and Nos2. The expression of Ccnd1, Tgfb1, Tgfb1r1 and Il10 in the liver was upregulated over the course of 3 days after splenectomy. see more Monitoring of the liver macrophage populations in splenectomized animals revealed a statistically significant increase in the proportion of CD68-positive cells in the liver (as compared with sham-operated controls) detectable at 24 h and 48 h after the surgery. The difference in the liver content of CD68-positive cells between splenectomized and sham-operated animals evened out by day 3 after the surgery. No alterations in the liver content of CD163-positive cells were observed in the experiments. A decrease in the proportion of CD206-positive liver macrophages was observed at 48 h after splenectomy. The splenectomy-induced hepatocyte proliferation is described by us for the first time. Mechanistically, the effect is apparently induced by the removal of spleen as a major source of Tgfb1 (hepatocyte growth inhibitor) and subsequently supported by activation of proliferation factor-encoding genes in the liver.Wnt/FZD signalling activity is required for spinal cord development, including the dorsal-ventral patterning of the neural tube, where it affects proliferation and specification of neurons. Wnt ligands initiate canonical, β -catenin-dependent, signaling by binding to Frizzled receptors. However, in many developmental contexts the cognate FZD receptor for a particular Wnt ligand remains to be identified. Here, we characterized FZD10 expression in the dorsal neural tube where it overlaps with both Wnt1 and Wnt3a, as well as markers of dorsal progenitors and interneurons. We show FZD10 expression is sensitive to Wnt1, but not Wnt3a expression, and FZD10 plays a role in neural tube patterning. Knockdown approaches show that Wnt1 induced ventral expansion of dorsal neural markes, Pax6 and Pax7, requires FZD10. In contrast, Wnt3a induced dorsalization of the neural tube is not affected by FZD10 knockdown. Gain of function experiments show that FZD10 is not sufficient on its own to mediate Wnt1 activity in vivo. Indeed excess FZD10 inhibits the dorsalizing activity of Wnt1. However, addition of the Lrp6 co-receptor dramatically enhances the Wnt1/FZD10 mediated activation of dorsal markers. This suggests that the mechanism by which Wnt1 regulates proliferation and patterning in the neural tube requires both FZD10 and Lrp6.The COVID-19 pandemic has highlighted the importance of rapid, cost effective, accurate, and non-invasive testing for viral infections. Volatile compounds (VCs) have been suggested for several decades as fulfilling these criteria. However currently very little work has been done in trying to diagnose viral infections using VCs. Much of the work carried out to date involves the differentiation of bacterial and viral sources of infection and often the detection of bacterial and viral co-infection. However, this has usually been done in vitro and very little work has involved the use of human participants. Viruses hijack the host cell metabolism and do not produce their own metabolites so identifying virus specific VCs is at best a challenging task. However, there are proteins and lipids that are potential candidates as markers of viral infection. The current understanding is that host cell glycolysis is upregulated under viral infection to increase the available energy for viral replication. There is some evidence that viral infection leads to the increase of production of fatty acids, alkanes, and alkanes related products.
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